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PubMed1999

Heritable coagulopathies in pregnancy.

UNLABELLED: Heritable coagulopathies are leading causes of maternal thromboembolism and are associated with an increased risk of maternal and perinatal morbidity and mortality. The most common of these disorders are antithrombin III deficiency, protein C deficiency, protein S deficiency, activated protein C resistance resulting from the factor V Leiden mutation, elevated prothrombin activity associated with a mutation in the prothrombin gene, and hyperhomocystinemia. The maternal risk of a thromboembolic episode is increased by a factor of eight in the presence of any of these heritable states. In addition, the relative risk for a stillbirth in the presence of one of these disorders is 3.6. These conditions are also associated with intrauterine growth retardation and preeclampsia. Proper management of heritable coagulopathies during pregnancy is essential to reduce the risk of these serious sequelae. Patients with newly diagnosed deep-vein thromboses or pulmonary emboli should be treated with therapeutic levels of unfractionated or low molecular weight heparin, followed by subsequent prophylactic heparin therapy. All patients with a history of thromboembolism before pregnancy or evidence of any of these coagulopathies may be offered prophylactic therapy with low molecular weight heparin. Patients with antithrombin III deficiency should receive full therapeutic heparin therapy for the entire pregnancy, irrespective of their thromboembolic history. Postpartum therapy with either heparin or warfarin is required in all cases. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians LEARNING OBJECTIVES: After completion of this article, the reader will be able to describe the various heritable coagulopathies that can complicate pregnancy, to state the potential adverse effects of heritable coagulopathies in pregnancy, and to explain the management of heritable coagulopathies during pregnancy.

Activated Protein C Resistance↗
PubMed1993

Antithrombin-III plasma activity during and after prolonged use of heparin in unstable angina.

Heparin effectively prevents the complications of unstable angina but disease reactivation has been documented following its discontinuation. To investigate whether this could be related to antithrombin-III depletion, 50 patients with unstable angina had serial determinations of activated partial thromboplastin time and of the plasma levels of heparin, antithrombin-III activity and of the thrombin-antithrombin-III complex before, during and, in a subgroup of 8 patients, 4 hours after heparin discontinuation. Heparin was administered intravenously at therapeutic doses for a mean of 7.6 +/- 4.1 days. Plasma antithrombin-III activity decreased rapidly from 1.05 +/- 0.03 to 1.0 +/- 0.03 U/ml (p < 0.03) following heparin initiation with no further significant subsequent decrease. Antithrombin-III activity returned to the control values 4 hours after the discontinuation of heparin. Thus, heparin treatment is associated with small, non-cumulative and rapidly reversible decrease in antithrombin-III activity. Reactivation of unstable angina after discontinuation of heparin must be explained by a mechanism other than antithrombin-III deficiency.

Angina, Unstable↗
PubMed1994

Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families.

We studied the molecular basis and genetic heterogeneity of hereditary antithrombin (III) deficiency in nine Dutch families. Polymerase chain reaction (PCR) amplification and direct sequencing of all antithrombin gene exons and flanking intronic regions identified mutations in eight families. Given the opportunity to correlate the molecular basis with survival, we addressed the relevance of molecular defects to mortality in inherited antithrombin deficiency. The defects included single nucleotide deletions (7671 del G, 7768-69 del G) and insertions (5501 ins A, 2463 G-->TC) that lead to frameshifts, a single base substitution [5381 C-->T (129Arg-->stop)] leading to a premature termination codon, and single base substitutions resulting in amino acid substitutions [2652 A-->C (63Tyr-->Ser), 13380 T-->C (421Ile-->Thr), and 13407 G-->T (430Cys-->Phe)]. All affected individuals were heterozygous for the defects. Previously we found in Dutch families that antithrombin deficiency did not lead to higher mortality compared with the general population. In accordance with these findings, we observed no excess mortality in the nine families [Observed:Expected, 52:52.6; standardised mortality ratio (SMR) 1.0, 95% confidence interval (CI), 0.7-1.3]. Our findings confirmed a considerable genetic heterogeneity underlying antithrombin deficiency. We therefore concluded that the lack of excess mortality in these families is not caused by a Dutch mild defect. We suggest that the longevity is not affected by molecular defects in the antithrombin gene and hypothesize that differences in mortality or natural history between families most likely result from other (genetic) risk factors.

Antithrombin III↗
PubMedDate not supplied

[Antithrombin III in 86 patients with venous thrombosis (author's transl)].

Antithrombin III concentration was studied in 86 patients with recurrent or extensive venous thrombosis. Two of them were found to have an hereditary antithrombin III deficiency. 25 patients receiving heparin therapy had low antithrombin III concentration. After stopping heparin treatment antithrombin rose to a normal level. Pathological antithrombin III modifications are recalled (synthesis decrease in liver diseases, intra vascular consumption during active venous thrombosis). Antithrombin III decreased activity induced by heparin treatment is pointed out.

Antithrombin III↗
PubMed2001

Thrombophilic factors in chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTE-PH) is an infrequent cause of pulmonary hypertension that develops in 0.1-0.2% of patients who survive after an acute venous thromboembolic event. According to the largest series so far reported, 15-30% of patients with diagnosis of CTE-PH have an underlying congenital or acquired hypercoagulable state. To determine the prevalence of thrombophilic factors in our population, we analyzed 24 patients admitted to our institution between November 1992 and March 2000 fulfilling criteria for CTE-PH. Eighteen patients disclosed abnormal results in the screening for thrombophilia. The presence of antiphospholipid antibodies (lupus anticoagulant and/or anticardiolipin antibodies) was the abnormality most frequently found (12 out of 24 patients). We found hyperhomocysteinaemia in 7/14, true protein S deficiency in 1/10, protein C deficiency in 1/13, activated protein C resistance in 1/22, antithrombin III deficiency in 1/24, and prothrombin gene G20210A mutation in 1/18 patients. Factor V Leiden was normal in all 18 patients studied. Five patients (20.8%) disclosed more than one thrombophilic abnormality. In conclusion, contrary to the largest series of patients with CTE-PH so far reported, we found that 75% of patients with CTE-PH presented at least one thrombophilic risk factor, being antiphospholipid antibodies in 50% of the cases. We recommend a thorough screening for thrombophilia in all patients with diagnosis of CTE-PH.

Activated Protein C Resistance↗
PubMedDate not supplied

Antithrombin III levels in pregnancy induced hypertension.

BACKGROUND: Antithrombin III deficiency is common as well as severe in both consumptive coagulopathy and conditions such as pregnancy induced hypertension. We determined antithrombin III levels in women suffering from pregnancy induced hypertension to determine its usefulness in assessing severity of the disease and outcome. METHODS: Forty-five pregnant women with mild and severe forms of pregnancy induced hypertension and 18 women with normal pregnancies matched for gestational age formed the study population. Fasting blood samples were collected and the plasma separated. Antithrombin III levels were estimated by the kinetic Berichrom antithrombin III method. RESULTS: The mean (SD) antithrombin III levels [0.76 (0.233) IU/ml] were significantly lower in pregnancy induced hypertension compared to the control group [0.97 (0.234) IU/ml]. Low antithrombin III and high diastolic blood pressure (> 110 mmHg) were related to poor pregnancy outcome in primigravidae. CONCLUSION: Mean antithrombin III levels were lower in pregnancy induced hypertension compared to a control group of women especially those who were primigravidae and had a diastolic blood pressure > 110 mmHg. Since low antithrombin III levels and a high diastolic blood pressure result in adverse pregnancy outcome monitoring of antithrombin III levels in pregnancy induced hypertension may help in assessing foetal jeopardy.

Adult↗
PubMed1981

[Pathogenetic mechanism and clinical relevance of acquired anti-thrombin III deficiency in internal medicine (author's transl)].

In three different disease entities associated with acquired antithrombin III (AT III) deficiency some of the pathogenetic mechanisms were studied. In liver cirrhosis (23 patients) the AT III level was closely correlated to the activity of hepatocellular synthesized clotting factors, indicating decreased AT III synthesis. In glomerular proteinuria (20 patients not on steroid therapy) the plasma level of AT III correlated inversely to the renal AT III clearance. In contrast to liver cirrhosis and proteinuria, in septicaemia (33 patients) the ratio between AT III antigen (radial immunodiffusion) and functional AT III (heparin cofactor assay using a chromogenic substrate) demonstrated an excess of AT III antigen probably due to inactive AT III-enzyme complexes. Therefore consumption of AT III appears to be an important cause of AT III deficiency in septicaemia. There was an inverse correlation between this ratio and the plasma AT III activity. It is well documented that congenital AT III deficiency predisposes to deep venous thrombosis (DVT) and sometimes to disseminated intravascular coagulation. A similar clinical relevance may be assumed for an acquired AT III deficiency, though so far a relationship between AT III deficiency and DVT has been only established in the nephrotic syndrome.

Antithrombin III Deficiency↗
PubMed1998

[Combined hemostatic defects in family members of symptomatic carriers of Leiden mutations of factor V].

The aim of the study was to determine the frequency of additional prothrombotic defect in family members of 14 symptomatic, heterozygous carriers of factor V Leiden mutation (FV Leiden). The FV Leiden was found in fifty-five from among 127 persons (43%). Thirty-two from 53 (68%) family carriers of FV Leiden had venous thromboembolic disease at the time of examination. Combined defects were found in 6 out of 14 families (in 4 families coexistence of FV Leiden mutation with protein S deficiency, in 1 with G20210 A mutation of prothrombin gene and in 1 with antithrombin III deficiency). Until now 63% (7/11) of combined defect carriers (mean age 48.5 years) and 59% (24/42) of heterozygous FV Leiden carriers (mean age 52.2 years) have been symptomatic. The thrombosis-free survival (Kaplan-Maier analysis) was comparable in combined and in single defect carriers groups.

Antithrombin III Deficiency↗
PubMed2005

No increase in rejection or graft loss in kidney transplant recipients with thrombophilia treated with anticoagulation and triple immunosuppression.

INTRODUCTION: Recent studies from Europe have demonstrated that patients with end-stage renal disease who receive a kidney transplant are at an increased risk for rejection and graft loss when compared with patients who have no known thrombophilia. The role of anticoagulation has not been investigated in these patients. MATERIALS AND METHODS: We prospectively tested patients who were evaluated for a kidney transplant for 8 thrombophilias, protein S and C deficiencies, factor V Leiden mutation, antithrombin III deficiency, anticardiolipin antibody, lupus anticoagulant, prothrombin gene mutation, and heparin-induced platelet antibody (HIPA). Patients with any identified thrombophilia received heparin or argatroban (for HIPA (+) patients) followed by coumadin for 1 year after transplantation. Triple therapy included cyclosporine, prednisone, and CellCept (Roche Pharmaceuticals, Nutley, NJ, USA). Sensitized, black, or repeat transplantation patients received induction with an interleukin (IL)-2 inhibitor. Data were collected in a retrospective manner. Rejection was biopsy-proven. RESULTS: Of the 112 transplant recipients who were tested for thrombophilia, 37 had 1 or more thrombophilia and 75 had no thrombophilia identified. Twenty-six patients received heparin and 11 received argatroban. There were no differences in recipient age, cold storage time, graft loss, HLA match, rejection episodes, 1-year graft survival, or serum creatinine level at 1 year. Significant differences were noted in posttransplantation bleeding, 35% versus 5%, and delayed graft function, 32% versus 15%, in patients with thrombophilia versus no thrombophilia, respectively. CONCLUSION: This is the first study to demonstrate that there is no increase in rejection or graft loss in kidney transplant recipients with thrombophilia when treated with anticoagulation and triple immunosuppression.

Anticoagulants↗
PubMed1999

[Ischemic colitis associated with antithrombin deficiency].

Colonic ischemia is one of the more common disorders of the colon in elderly people; the ischemic colitis can affect young people too. The splenic flexure, the descending colon and the sigmoid are the parts most commonly involved. Only in some cases it is possible to identify the specific cause of colonic ischemia. We report a case of ischemic colitis associated with antithrombin III deficiency.

Antithrombin III Deficiency↗
PubMed1985

Thromboembolism.

The overall incidence of venous thromboembolism is about 0.7 per thousand maternities, but pulmonary embolus is currently the single most common cause of maternal mortality. Major risk factors are operative delivery, age, multiparity and previous thromboembolism. Because of the risks in anticoagulant therapy and the difficulties of clinical diagnosis, it is essential to use objective tests, usually venography for deep-vein thrombosis and lung scan for pulmonary embolus. The acute phase will normally be treated with a continuous infusion of heparin, followed by subcutaneous heparin, given until at least six weeks post-delivery. Warfarin may be substituted after the first week post-delivery. In contrast to the treatment of other forms of thromboembolism, patients with artificial heart valves should be managed with warfarin until 36 weeks of pregnancy. Although the fetal risks in warfarin therapy are greater than those of subcutaneous heparin, the obvious alternative, subcutaneous heparin, does not provide adequate prophylaxis against thromboembolism. In patients who have had venous thromboembolism in the past, the maternal risks do not justify prolonged prophylaxis with subcutaneous heparin as usually given (20 000 units per day) throughout pregnancy. Further clinical trials are necessary to select the best alternatives. Antithrombin III deficiency should be managed with subcutaneous heparin taken from before conception until at least one week post-delivery, when warfarin therapy can be recommended. In addition, the labour should be covered with antithrombin III concentrate.

Adult↗
PubMed1982

Antithrombin III transfusion in patients with hepatic cirrhosis.

This study was designed to examine the effect of selective correction of antithrombin III activity on the increased turnover of fibrinogen, which occurs in patients with liver cirrhosis supposedly due to disseminated intravascular coagulation. Human antithrombin III concentrates were therefore transfused in seven patients with cirrhosis and antithrombin III deficiency (less than 80%). Fibrinogen half-life and the fractional catabolic rate constant were calculated from the turnover of 125I-fibrinogen which was represented by a two-compartment model. Prior to antithrombin III transfusion, 125I-fibrinogen half-life was 76.7 +/- 15.2 h and the fractional catabolic rate constant was 0.33 +/- 0.11 of the plasma fibrinogen pool per day. In six healthy adult controls these values were significantly different: 109.4 +/- 8.8 h and 0.19 +/- 0.01 respectively. Correction of antithrombin III activity with human antithrombin III concentrate reduced the increased turnover of radiolabelled fibrinogen to normal. The 125I-fibrinogen half-life became 108.4 +/- 17.6 h and the fractional catabolic rate constant decreased to 0.23 +/- 0.06. These observations indicate that decreased antithrombin III activity contributes in an important way to the increased 125I-fibrinogen turnover in patients with cirrhosis and this might reflect intravascular coagulation.

Adult↗
PubMed1993

Controlled trial of antithrombin III supplementation in fulminant hepatic failure.

Patients with fulminant hepatic failure have severe circulatory disturbances which may be due to fibrin and cellular plugs in micro-vessels which are a consequence of intravascular coagulation and which can lead to multiorgan failure. Since antithrombin III supplementation has been shown to be beneficial in animal models of septic shock with disseminated intravascular coagulation, a controlled study was performed to investigate the effect of antithrombin III supplementation in fulminant hepatic failure. Twenty-five patients in grade III or IV coma were selected on the basis of evidence of sepsis, intravascular coagulation and a high risk of developing multiorgan failure. Thirteen patients received 3000 units of antithrombin III (Kybernin P; Behringwerke), followed by a further 1000 units every 6 h. Antithrombin III activity increased from 0.26 +/- 0.04 SE U/ml to 0.82 +/- 0.07 U/ml at 3 h post infusion (normal range 0.80-1.20 U/ml) and remained greater than 0.80 U/ml throughout the study without any apparent increase in the frequency of bleeding. However, survival was not improved and markers of intravascular coagulation remained similar between the two groups. Thus, although the antithrombin III deficiency in fulminant hepatic failure can be corrected by supplementation with antithrombin III concentrate, its use in the prevention of intravascular coagulation and to avoid microvessel plugging needs to be studied at an earlier stage in the disease.

Adolescent↗
PubMed1998

[MALT lymphoma of the left lacrimal and mammary glands, liver cirrhosis caused by HCV and type II cryoglobulinemia].

We describe a case of MALT (mucosa-associated lymphoid tissue) lymphoma associated to post-hepatitis C liver cirrhosis, type II cryoglobulinaemia, gastrointestinal bleedings and thromboses. HCV infection justified the association between the first three pathologies, while gastrointestinal bleedings and thromboses were respectively attributed to portal hypertension secondary to liver cirrhosis and to some thrombophilic conditions. Among the latter there was also an antithrombin III deficiency. The singularity of the case and some difficulties met in its treatment, justify the report.

Aged↗
PubMed1986

[Fibrinolysis defects in patients with recurrent thromboses].

In 53 patients suffering from recurrent thrombosis various hemostaseological parameters were investigated. In 91 per cent of the patients spontaneous fibrinolytic activity was decreased. Decreased or lacking activity of the fibrinolytic system following venous occlusion was found in 48 per cent. In most cases, the concentration of alpha 2-macroglobulin was reduced. This was most pronounced in patients with antithrombin III deficiency. In nearly all cases the concentration of alpha 2-antiplasmin was enhanced. Prospective long-term studies on the importance of defective fibrinolysis are required.

Antithrombin III Deficiency↗
PubMed1985

Pst I polymorphism of the antithrombin III gene in a French population.

Pst I endonuclease fragment length polymorphism of the antithrombin III probe was studied in a French population. Among 25 subjects tested, 15 were found heterozygous at the Pst I site, so that this polymorphism might serve as a useful markers of antithrombin III gene in families with antithrombin III deficiency.

Antithrombin III↗
PubMed1993

[Neonatal testicular ischemic necrosis without torsion, associated with antithrombin III deficit].

There have been few reports of neonatal ischemic necrosis of the testis without torsion of the spermatic cord, which may be caused either by compression in utero or by transient torsion of the spermatic cord resolving spontaneously before surgery. The patient reported herein developed an inflammatory swelling of the right scrotum and an ecchymotic plaque over the left thigh at four days of age. Ischemic necrosis of the right testis without torsion was found upon surgery. When the patient was ten days of age, he developed an inflammatory swelling in the left scrotum; ischemic necrosis of the left testis without torsion was again found upon surgery. Thrombosis of the spermatic vessels was suspected. Postoperatively, ecchymotic and necrotic skin lesions developed, followed by pulmonary embolism and cerebral thrombosis. Outcome was fatal. Hematologic tests in the neonate and his parents established the diagnosis of inherited antithrombin III deficiency. Ischemic necrosis of the testes was thus probably due to hypercoagulability. No similar cases have been reported to date.

Antithrombin III Deficiency↗